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Soman (GD) nerve agent The third military nerve agent developed by Germany in the 1930s, but
never produced in any meaningful quantity, soman nerve agent was later
classified by the US military and NATO with the designation GD, after the
“German” series of nerve agents GA and GB. (There is no nerve agent
with the GC classification, as this was already taken by the US military medical
code for gonorrhea.) Soman is a colorless liquid and has been described having
an odor of fruit or camphor. Although chemically it is not far removed from
sarin, soman is relatively persistent with a lower volatility rating. Thus,
soman was often referred to as an intermediate volatile agent. The toxicity of
soman inhaled (vapor) is estimated (median lethal dose, or LD50) to
be 50mg-min/m3, or 350mg through the skin. How soman got its name is still
uncertain, but may derive from the Latin for “bludgeon” or the Greek
for “sleep.”  
The toxic principle of soman is its ability to inhibit
acetylcholinesterase (AChE), the body’s enzyme required for proper nerve
transmission at the molecular level. Increased levels of acetylcholine produce
exaggerated levels of bodily secretions and muscular twitching, as well as
pronounced effects on the cardiovascular and central nervous systems. While
death from respiratory paralysis can occur as a consequence, victims are also
prone to asphyxiate due to mucous and salivary excretions from the upper
respiratory tree. Without timely medical intervention and follow-up treatment,
those who do survive exposure to large doses of nerve agents can suffer
permanent neurological damage. Because of soman’s propensity to quickly
“age” AChE, the soman-inhibited enzyme is particularly difficult to
treat with oxime drugs, such as pralidoxime chloride (2-PAM-Cl). 
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